Observational studyNature communications2024
Lewy body pathology exacerbates brain hypometabolism and cognitive decline in Alzheimer's disease.
Observational study in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Longitudinal Cognitive Function in Progressive Supranuclear Palsy-A Review of the Evidence for Progression.Movement disorders clinical practice · 2026Review
- Network-dependent remote effects and local tau burden jointly shape neuronal dysfunction in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- TMEM106B is a selective modulator of TDP-43 pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Plasma proteome profiling identified biomarkers for the differential diagnosis and molecular staging of neurodegenerative dementias.Nature aging · 2026Article
- Plasma brain-derived p-Tau217 outperforms other p-Tau species in detecting abnormal brain amyloid in an Asian cohort of older people with cerebrovascular disease burden.The journal of prevention of Alzheimer's disease · 2026Observational
- Neuropsychological Profile and Cognitive Trajectories of Patients With Biomarker Evidence of Alzheimer Disease or Dementia With Lewy bodies.Neurology · 2026Article
- Deep learning-based MRI analysis reveals Lewy body co-pathology accelerates brain aging in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Contributions of the Alzheimer's Disease Neuroimaging Initiative to advancing AD research: a targeted review of recent publications.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- CSF alpha-Synuclein Seed Amplification Assay results in routine clinically collected samples.Journal of Parkinson's disease · 2026Article
- In vivo-measured Lewy body pathology is associated with neuropsychiatric symptoms across the Alzheimer's disease continuum.Molecular psychiatry · 2026Article
- Discordance of Dopaminergic Dysfunction and Subcortical Atrophy by α-Synuclein Status in Sporadic and Genetic Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Biological classification of memory clinic patients.Brain : a journal of neurology · 2026Article
- Metabolic brain networks in dementia with Lewy bodies: from prodromal to manifest disease stages.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- α-synuclein positivity is associated with decline in brain microstructure in the Alzheimer's disease spectrum.Alzheimer's research & therapy · 2026Article
- Sex-Specific Associations of α-Synuclein Pathology With Tau Accumulation.JAMA network open · 2026Article
- A quantitative DOPA decarboxylase biomarker for diagnosis in Lewy body disorders.Nature medicine · 2026Article
- Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Tau in Alzheimer's disease: Shaping the future patient journey.The journal of prevention of Alzheimer's disease · 2026Review
- Alpha-synuclein seeding activity in postmortem tissues from patients with diffuse and isolated Lewy bodies.Acta neuropathologica communications · 2026Article
- Impact of Lewy body and limbic-predominant TDP-43 neuropathology on cognitive and neuropsychiatric trajectory in Alzheimer's disease: a retrospective neuropathological study.Frontiers in aging neuroscience · 2026Article
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Funding
Abstract
Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. This study examined whether LB pathology exacerbates AD-related disease progression in 795 cognitively impaired individuals (Mild Cognitive Impairment and dementia) from the longitudinal multi-center observational ADNI cohort. Participants were on average 75 years of age (SD = 7.89), 40.8% were female, 184 (23.1%) had no biomarker evidence of AD/LB pathology, 39 (4.9%) had isolated LB pathology (AD-LB+), 395 (49.7%) had only AD pathology (AD+LB-), and 177 (22.3%) had both pathologies (AD+LB+). The AD+LB+ group showed worst baseline performance for most cognitive outcomes and compared to the AD+LB- group faster global cognitive decline and more cortical hypometabolism, particularly in posterior brain regions. Neuropathological examination (n = 61) showed high sensitivity (26/27, 96.3%) and specificity (27/28, 96.4%) of the SAA-test. We showed that co-existing LB-positivity exacerbates cognitive decline and cortical brain hypometabolism in AD. In vivo LB pathology detection could enhance prognostic evaluations in clinical practice and could have implications for clinical AD trial design.
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